Plasma somatostatin and gastrointestinal peptides in Alzheimer's disease and vascular dementia.
(41/443)
Few markers distinguish between different dementia types. As dementia affects many body systems outside the central nervous system, we investigated gastrointestinal regulatory peptides as possible disease markers in Alzheimer's Disease (AD) and vascular dementia (VaD). Subjects with mild-to-moderate dementia were diagnosed as probable AD and VaD according to defined criteria. Gastrointestinal peptides were stimulated using a standardized meal test, administered after an overnight fast to 58 dementia patients (40 AD, 18 VaD) and 47 controls matched for age and sex. Blood samples were taken at designated time intervals, and basal and stimulated plasma concentrations of eleven peptides were determined by radio-immunoassay. Results were analysed using the Kruskal-Wallis one-way analysis of variance; the Mann-Whitney U test was used in post hoc analysis where appropriate. There were significant differences in somatostatin levels but in none of the other peptides. Basal somatostatin was significantly increased in VaD compared to controls (p<0.05), and AD (p<0.005). Maximum stimulated levels were significantly elevated in VaD compared to AD (p<0.01). Median basal and stimulated levels of somatostatin were increased in VaD compared to AD, but the overlap in individual values between the groups makes it unlikely to be useful in distinguishing the two types of dementia. (+info)
A study of platelet organelles and membrane glycoprotein in patients with Binswanger's disease.
(42/443)
OBJECTIVE: To discuss the possible role of platelets in Binswanger's disease by studying the changes of organelles and membrane glycoprotein in platelets. METHODS: The organelles (dense bodies, alpha granules, and mitochondria) within platelets were measured with transmission electron microscopy in 25 patients with Binswanger's disease and matched controls, while alpha granule membrane glycoprotein CD62 and lysosomal integral membrane glycoprotein CD63 on platelet membrane were analyzed by flow cytometry. RESULTS: The percentage of CD62-positive platelets was 3.6% +/- 2.1% and 5.7% +/- 2.4% in controls and in patients, respectively (P < 0.01). The percentage of CD63 expression platelets was 3.1% +/- 2.2% and 3.2% +/- 2.3% in controls and patients, respectively (P > 0.05). When compared with controls, platelets of patients contained fewer alpha granules (P < 0.01), and had no changes in dense bodies and mitochondria (P > 0.05). CD62 levels were different among patients with regarding to the degree of white matter low attenuation. CONCLUSION: There is selective degranuation of platelets in patients with Binswanger's disease and the abnormalities of platelet secretion may play a role in the pathophysiology of this illness. (+info)
Standardized Mini-Mental State Examination. Use and interpretation.
(43/443)
OBJECTIVE: To review administration of the Standardized Mini-Mental State Examination (SMMSE) for dementia and depression and to evaluate how well it interprets older people's cognitive function. QUALITY OF EVIDENCE: Literature from January 1990 to December 1999 was searched via MEDLINE using the MeSH headings Alzheimer Disease, Vascular Dementia, Lewy Bodies, and Depression. Several studies have described the reliability and validity of the SMMSE. MAIN MESSAGE: The SMMSE, a standardized approach to scoring and interpreting older people's cognitive function, provides a global score of cognitive ability that correlates with daily function. Careful interpretation of results of the SMMSE, together with history and physical assessment, can assist in differential diagnosis of cognitive impairment resulting from Alzheimer's disease, vascular dementia, dementia with Lewy bodies, or depression. Repeated measurements can be used to assess change over time and response to treatment. CONCLUSION: The SMMSE is a valuable tool for family doctors who are often the first medical professionals to identify changes in patients' cognitive function. The SMMSE requires little time to complete and is a key component of a comprehensive dementia workup. Determining whether a patient has dementia is important because there are now effective medications that are most beneficial if started early. (+info)
Efficacy and safety of risperidone oral solution in agitation associated with dementia in the elderly.
(44/443)
BACKGROUND: Behavioral and psychological symptoms in dementia (BPSD) contribute to caregiver burden and institutionalization of elderly. Neuroleptics are prescribed to control agitation. Side effects of typical neuroleptics are harmful, making atypical neuroleptics an indication. OBJECTIVES: To evaluate efficacy and tolerability of risperidone oral solution (ROS) given once daily to demented elderly outpatients with BPSD (agitation). METHOD: Patients (n=26), 76.35+/-8.63 years, Diagnostic and Statistical Manual of Mental Disorders 4th ed. (DSM-IV) criteria for dementia. RSO was given, starting dose of 0.25 mg and increments of 0.25 mg every week. Mini-Mental State Examination (MMSE) assessed cognitive status, Behavioral and Emotional Activities Manifested in Dementia (BEAM-D) and Clinical Global Impression (CGI) measured BPSD, Extrapiramidal Symptom Rating Scale (ESRS) evaluated extrapyramidal symptoms. Cardiovascular side effects were evaluated clinically. RESULTS: There was a 26% reduction in agitation and no cardiovascular side effects in the range from 1.0 to 1.25 mg. Side effects were more prevalent above 2.5 mg. CONCLUSION: Risperidone oral solution improved agitation with good tolerability from 0.5 to 1.25 mg. A single dose with increments of 0.25 mg may be more acceptable to patients and caregivers. (+info)
Pravastatin improves cerebral vasomotor reactivity in patients with subcortical small-vessel disease.
(45/443)
BACKGROUND AND PURPOSE: Recent investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment. METHODS: In 16 patients (mean age 68+/-10 years) with subcortical small-vessel disease, cerebral vasomotor reactivity was tested using TCD insonating the middle cerebral artery. Cerebral blood flow velocity (CBFV) increase after bolus injection of 1 g acetazolamide was determined before and after 2-month treatment with pravastatin sodium 20 mg daily. RESULTS: Relative CBFV increase was significantly greater after pravastatin treatment (41.9+/-23.7% versus 55.7+/-18.3%, P=0.004). Comparison of CBFV at rest before and after treatment with pravastatin did not show significant differences. There was a strong negative correlation between the pravastatin-induced enhancement of vasomotor reactivity and the pretreatment CBFV increase (beta=-0.64, P=0.019). No associations were found between the effect of pravastatin on vasomotor reactivity and pretreatment levels or changes of LDL cholesterol. CONCLUSIONS: This pilot study provides the first evidence for a significant improvement of cerebral vasomotor reactivity by statin therapy in patients with cerebral small-vessel disease. The results may help to elucidate the preventive effect of statins and provide insights into the pathophysiology of cerebral small-vessel disease. (+info)
Caudoputamen is damaged by hypocapnia during mechanical ventilation in a rat model of chronic cerebral hypoperfusion.
(46/443)
BACKGROUND AND PURPOSE: Postoperative brain dysfunction, such as delirium, is a common complication of anesthesia and is sometimes prolonged, especially in patients with cerebrovascular disease. In the present study we investigated the effect of hypocapnia during anesthesia on neuronal damage using a rat model of chronic cerebral hypoperfusion. METHODS: Chronic cerebral hypoperfusion was induced by clipping the bilateral common carotid arteries in male Wistar rats. Fourteen days after the operation, these animals were mechanically ventilated for 2 hours and then kept in suitable conditions for an additional 14 days. Twenty-four rats were assigned to 4 groups: those with chronic cerebral hypoperfusion with either hypocapnia or normocapnia during anesthesia, and those given sham operation with either hypocapnia or normocapnia. White matter lesions in the brain sections were evaluated with Kluver-Barrera staining. Proliferation of glial cells was estimated with the use of immunohistochemistry of glial fibrillary acidic protein, a marker for astroglia, and CD11b, a marker for microglia. Computer-assisted morphometry was applied to the immunohistochemical results of microtubule-associated protein 2 to evaluate the loss of neurons. RESULTS: The histological damage was localized almost exclusively in the white matter in the rats subjected to chronic cerebral hypoperfusion but without hypocapnia. Neuronal damage and astroglial proliferation occurred with aggravated white matter lesions in the caudoputamen in the rats with chronic cerebral hypoperfusion and hypocapnia. No lesions were observed in sham-operated rats with either hypocapnia or normocapnia. CONCLUSIONS: These results indicate that hypocapnia during anesthesia causes tissue damage in the caudoputamen, which may be responsible for long-lasting postoperative delirium in patients with stroke and/or dementia. (+info)
MRI predictors of cognition in subcortical ischemic vascular disease and Alzheimer's disease.
(47/443)
BACKGROUND: Causes of cognitive impairment in subcortical ischemic vascular disease (SIVD) are less well understood than in AD, but have been thought to result from direct effects of subcortical lacunes and white matter lesions, perhaps related to disruption of important cortical-subcortical pathways. OBJECTIVE: To examine the relation between cognitive abilities and quantitative MRI measures of subcortical cerebrovascular disease and cortical and hippocampal atrophy. METHODS: Subjects were 157 participants in a multicenter study of SIVD and AD who included cognitively normal, cognitively impaired, and demented individuals with and without subcortical lacunar infarcts. Dependent variables were neuropsychological tests of global cognitive function, memory, language, and executive function. Independent variables were quantitative MRI measures of volume of lacunar infarcts in specific subcortical structures, volume of white matter lesion (WML), volume of cortical gray matter (cGM), and total hippocampal volume (HV). Multiple regression analyses were used to identify MRI predictors of cognition. RESULTS: Subcortical lacunes were not related to cognitive measures independent of effects of other MRI variables. WML was independently related to selected, timed measures. HV and cGM were strong and independent predictors of cognitive variables, with effects that did not differ in subjects with and without subcortical lacunes. CONCLUSIONS: Results suggest that cognitive impairment associated with subcortical ischemic vascular disease is primarily a result of associated hippocampal and cortical changes. (+info)
Twenty-four-hour blood pressure and MRI as predictive factors for different outcomes in patients with lacunar infarct.
(48/443)
BACKGROUND AND PURPOSE: A long-term follow-up study was conducted in patients with lacunar infarct to assess how 24-hour blood pressure monitoring values and MRI findings, in particular lacunar infarcts and diffuse white matter lesions, can predict subsequent development of dementia and vascular events, which include cerebrovascular and cardiovascular events. METHODS: One hundred seventy-seven patients were tracked for a mean of 8.9 years of follow-up. Documented events comprise the development of dementia and the occurrence of vascular events. The predictors for developing dementia and vascular events were separately evaluated by Cox proportional hazards analysis. RESULTS: Twenty-six patients developed dementia (0.17/100 patient-years). Male sex (relative risk [RR], 4.2; 95% CI, 1.2 to 14.7), cognitive impairment (RR, 3.0; 95% CI, 1.0 to 8.5), confluent DWML (moderate: RR, 7.1; 95% CI, 1.6 to 31.5; severe: RR, 35.8; 95% CI, 7.2 to 177.3), and nondipping status (RR, 7.1; 95% CI, 2.2 to 22.0) were independent predictors for dementia. Forty-six patients suffered from vascular events (3.11/100 patient-years). Diabetes mellitus (RR, 5.7; 95% CI, 2.7 to 11.9), multiple lacunae (moderate: RR, 6.4; 95% CI, 2.5 to 15.8; severe: RR, 8.5; 95% CI, 3.1 to 23.3), and high 24-hour systolic blood pressure (>145 mm Hg versus <130 mm Hg) (RR, 10.3; 95% CI, 1.3 to 81.3) were independent predictors for vascular events. CONCLUSIONS: Predictors for developing dementia and vascular events appear to differ. Male sex, confluent diffuse white matter lesions, and nondipping status were independent predictors for subsequent development of dementia, while diabetes mellitus, multiple lacunae, and high 24-hour systolic blood pressure were independent predictors for vascular events. (+info)